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FM increases oxidative stress and mitochondrial damage in TNBC. The release of MDA (A) and GSH (B) in MCF7 cells. (C) Mitochondrial aggregation determined by immunofluorescence. (D) The protein expression of cyto C in MCF7 cells determined using western blot. **P<0.01, ***P<0.001.
Source publication
This study aimed to investigate the effects of formononetin on triple negative breast cancer (TNBC). Clinical samples were collected from patients with TNBC. Overall survival rates were evaluated using the Kaplan-Meier method. Gene expression was determined using immunohistochemistry, immunofluorescence and western blot. Cellular functions were det...
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... we determined the release of oxidative stress in TNBC. FM enhanced the effects of NP on the release of MDA and GSH (Figs 2A and B). FM enhanced mitochondrial aggregation induced by NP (Fig. 2C). ...
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... studies reveal that FM suppresses the progression of multiple myeloma via inducing oxidative stress. Then we determined the release of oxidative stress in TNBC. FM enhanced the effects of NP on the release of MDA and GSH (Figs 2A and B). FM enhanced mitochondrial aggregation induced by NP (Fig. 2C). Moreover, FM+NP markedly increased cyto C protein expression compared with the NP group (Fig. ...
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... of multiple myeloma via inducing oxidative stress. Then we determined the release of oxidative stress in TNBC. FM enhanced the effects of NP on the release of MDA and GSH (Figs 2A and B). FM enhanced mitochondrial aggregation induced by NP (Fig. 2C). Moreover, FM+NP markedly increased cyto C protein expression compared with the NP group (Fig. ...
Citations
Formononetin is a flavonoid compound with anti-tumor and anti-inflammatory properties. However, its low solubility limits its clinical use. We employed microfluidic technology to prepare formononetin-loaded PLGA-PEGDA microspheres (Degradable polymer PLGA, Crosslinking agent PEGDA), which can encapsulate and release drugs in a controlled manner. We optimized and characterized the microspheres, and evaluated their antitumor effects. The microspheres had uniform size, high drug loading efficiency, high encapsulation efficiency, and stable release for 35 days. They also inhibited the proliferation, migration, and apoptosis. The antitumor mechanism involved the induction of reactive oxygen species and modulation of Bcl-2 family proteins. These findings suggested that formononetin-loaded PLGA-PEGDA microspheres, created using microfluidic technology, could be a novel drug delivery system that can overcome the limitations of formononetin and enhance its antitumor activity.
Cerebral ischemia is a cerebrovascular disease with symptoms caused by insufficient blood or oxygen supply to the brain. When blood supplied is restored after cerebral ischemia, secondary brain injury may occur, which is called cerebral ischemia-reperfusion injury (CIRI). In this process, the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway plays an important role. It mediates neuroinflammation and participates in the regulation of physiological activities, such as cell proliferation, differentiation, and apoptosis. After CIRI, M1 microglia is activated and recruited by the damaged tissue. The inflammatory factors are produced by M1 microglia through the JAK/STAT pathway, eventually leading to cell apoptosis. Meanwhile, the JAK2/STAT3 signaling pathway and the expression of lipocalin-2 and caspase-3 could increase. In the pathway, phosphorylated JAK2 and phosphorylated STAT3 function of 2 ways. They not only promote the proliferation of neurons, but also affect the differentiation direction of neural stem cells by further acting on the Notch signaling pathway. Recently, traditional Chinese medicine (TCM) is a key player in CIRI, through JAK2, STAT3, STAT1 and their phosphorylation. Therefore, the review focuses on the JAK/STAT signaling pathway and its relationship with CIRI as well as the influence of the TCM on this pathway. It is aimed at providing the basis for future clinical research on the molecular mechanism of TCM in the treatment of CIRI.
